Table 1.

Evidence of the roles of noncoding RNA molecules in hyperoxia

RNA molecule	Type of RNA	Hyperoxic model	Outcome	Reference
miR-150	miRNA	Lung injury/newborn mice/95% O2/3–10 days	• Downregulated in hyperoxia • KO decreased lung injury	(Narasaraju et al. 2015)
		Lung injury/primary mouse lung epithelial cells, BEAS-2B and A549 cells/95% O2/12–72 h	• Cytoprotective effect	(Zhang et al. 2017a)
miR-876-3p	miRNA	Lung injury/newborn mice/85–100% O2/4–14 days Normal human bronchial epithelial/85% O2/24 h	• Downregulated in hyperoxia • Predicted protective effect against injury	(Lal et al. 2018)
miR-16	miRNA	Lung injury/isolated T2AECs/60% O2 /24 h	• Downregulated in hyperoxia • miR-16 mimics inhibited apoptosis and the TGF‐β/Smad2 and Jak/STAT3 pathways	(Li et al. 2018)
miR-34a	miRNA	Lung injury/newborn mice/100% O2/4 or 7 days Isolated T2AECs and MLE-12 cells/40–95% O2/4–48 h	• Silencing ameliorated apoptosis in vitro and in vivo • Overexpression aggravated injury	(Syed et al. 2017)
		Lung injury/newborn mice/85% O2/14 days MLg cells/85% O2/unspecified duration	• Upregulated in hyperoxia • Deletion protected against injury	(Ruiz-Camp et al. 2019)
miR-17	miRNA	Lung injury/newborn mice/70% O2/4–14 days	• Downregulated in hyperoxia • Downregulated STAT3 • Upregulation relieved pulmonary injury	(Zhang et al. 2020)
		Lung injury/newborn mice/85% O2/14 days	• Downregulated in hyperoxia • Downregulation was associated with lung injury	(Wang et al. 2020)
miR-185-5p	miRNA	Lung injury/mice/95% O2/24–72 h MLE-15 cells/95% O2/24–48 h	• Upregulated in hyperoxia • Upregulated RIP1 and RIP3 • Induced necroptosis and apoptosis	(Carnino et al. 2020)
miR-96	miRNA	OIR/newborn rats/cycling 10–50% O2 every 24 h/14 days Retinal vaso-obliteration/newborn rats/80% O2/5 days HRMECs/80% O2/1–48 h	• Downregulated in hyperoxia • Overexpression promoted vascular repair in vivo and protected against endothelial dysfunction in vitro	(Desjarlais et al. 2020)
miR-101-3p	miRNA	Lung injury/newborn mice/65% O2/7–14 days	• Overexpression mitigated injury • Downregulated HMGB3 and TGF-ß1/Smad3 axis	(Yuan et al. 2020)
miR-18a	miRNA	Lung injury/mouse/95% O2/7 days MLE-12 cells/95% O2/12–48 h	• Downregulated in hyperoxia • Overexpression prevented pyroptosis and relieved lung injury	(Zou et al. 2020)
miR-29b	miRNA	Plasma from preterm infants lung injury/newborn mice/85% O2/14 days	• Downregulated in hyperoxia • Improved alveolarization and decreased expression of ECM proteins	(Durrani-Kolarik et al. 2017)
miR-29a	miRNA	Lung injury/newborn mice/ > 90% O2/4 days	• Upregulated in hyperoxia • Inhibition alleviated injury	(Hu et al. 2020)
miR-199a-5p	miRNA	Lung injury/newborn mice/100% O2/7 days Mouse MLE-12 cells and RAW264.70 cells/95% O2/4–24 h	• Upregulated in hyperoxia • Mimic treatment worsened injury	(Alam et al. 2019)
miR-20b	miRNA	Lung injury/rats/95% O2/48 h	• Downregulated in hyperoxia • Overexpression downregulated Mfn1/2 and reduced apoptosis	(Mu et al. 2021)
miR-214	miRNA	Lung injury/newborn rats/95% O2/7 days Alveolar epithelial cells/85% O2/24 h	• Downregulated in hyperoxia • Overexpression restored alveolarization in vivo and decreased apoptosis in vitro	(Zhang et al. 2021b)
miR-421	miRNA	Lung injury/newborn mice/85% O2/7 days MLE-12 cells/85% O2/6 h	• Upregulated in hyperoxia • Downregulation was associated with alleviated injury • Mimic treatment abrogated Rian-mediated protection	(Tao et al. 2021)
miR-194-5p	miRNA	Lung injury/newborn mice/ > 90% O2/4 days BEAS-2B cells/95% O2/48 h	• Mediated hyperoxic injury • Upregulation blocked CASC2-mediated protection	(Ji et al. 2021)
miR‐181c‐5p	miRNA	HLMECs/80% O2/12–24 h	• Upregulated in hyperoxia • miR‐181c‐5p mimic downregulated NCAPG and enhanced apoptosis	(Wu et al. 2021)
miR-342-5p	miRNA	Lung injury/newborn mice/100% O2/4–7 days T2AECs and MLE-12 cells/95% O2/2–48 h	• Downregulated in hyperoxia • Overexpression and mimic treatment ameliorated injury	(Wen et al. 2021)
miR-299-3p	miRNA	OIR/newborn mice/75% O2/5 days	• Downregulated in hyperoxia • Overexpression reduced apoptosis	(Wang et al. 2022b)
FOXD3-AS1	lncRNA	Lung injury/primary mouse lung epithelial cells, BEAS-2B and A549 cells/95% O2/12–72 h	• Upregulated in hyperoxia in vivo and in vitro • Deletion is cytoprotective in vivo and in vitro	(Zhang et al. 2017a)
Xist	lncRNA	Lung injury/newborn mice/65% O2/7–14 days	• Upregulated in hyperoxia • Silencing protects against injury	(Yuan et al. 2020)
H19	lncRNA	Lung injury/newborn mice/70% O2/4–14 days	• Upregulated in hyperoxia • Silencing upregulated miR-17, downregulated STAT3, and relieved injury	(Zhang et al. 2020)
MEG3	lncRNA	Lung injury/mice/95% O2/7 days MLE-12 cells/95% O2/12–48 h	• Upregulated in hyperoxia • Knockdown inhibited NLRP3 inflammasome, caspase-1, and pyroptosis	(Zou et al. 2020)
MALAT1	lncRNA	BPD patients A549 cells 92% O2/48 h	• Upregulated in BPD • Downregulated in hyperoxia in vitro • Silencing promoted apoptosis	(Zhang et al. 2021a)
Rian	lncRNA	Lung injury/newborn mice/85% O2/7 days MLE-12 cells/85% O2/6 h	• Downregulated in vivo and in vitro • Overexpression downregulated miR-421 and alleviated injury	(Tao et al. 2021)
CASC2	lncRNA	Lung injury/newborn mice/ > 90% O2/4 days/10 days recovery in normoxia BEAS-2B cells/95% O2/48 h	• Poorly expressed in hyperoxic mice • Overexpression ameliorated lung injury in vivo • Inhibited apoptosis of epithelial cells in vitro	(Ji et al. 2021)
DLEU2	lncRNA	HLMECs/80% O2/12–24 h	• Downregulated in hyperoxia • Overexpression inhibited miR‐181c‐5p and hyperoxic damage	(Wu et al. 2021)
TUG1	lncRNA	OIR/newborn mice/75% O2/5 days	• Upregulated in hyperoxia • Knockdown reduced pathological alterations, apoptosis, inflammation, and miR-299-3p expression	(Wang et al. 2022b)

Abbreviations: CASC2, cancer susceptibility candidate 2; DLEU2, deleted in lymphocytic leukemia 2; ECM, extracellular matrix; FOXD3-AS1, FOXD3 antisense RNA 1; HMGB3, high mobility group box 3; HLMECs, human lung microvascular endothelial cells; HPMECs, human pulmonary microvascular endothelial cells; HRMECs, human retinal microvascular endothelial cells; Jak, Janus kinase; KO, knockout; MALAT1, metastasis-associated lung adenocarcinoma transcript; MEG3, maternally expressed 3; Mfn1/2, mitofusin 1/2; NCAPG, non-SMC condensin I complex subunit G; NLRP3, NLR family pyrin domain containing 3; OIR, oxygen-induced retinopathy; RIP1/3, receptor-interacting protein 1/3; Smad2, small mothers against decapentaplegic 2; STAT3, signal transducer and activator of transcription 3; TGF-β, transforming growth factor-β; TUG1, taurine up-regulated 1; T2AECs, type II alveolar epithelial cells; Xist, X-inactive specific transcript